Premium
February 2013
Author(s) -
John D. Nelson,
George H. McCracken
Publication year - 2013
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.23871
Subject(s) - citation , annals , computer science , information retrieval , library science , history , classics
When studying the requirements for CNS re-activation of CD81 T cells in (CD41 T cells-induced) experimental autoimmune encephalomyelitis or EAE, Ji and colleagues discovered that myelin basic protein (MBP) was presented to the infiltrating CD81 T cells by CD11b1 “Tip-dendritic cells” (tumornecrosis factor inducible nitric oxide synthase producing DCs), derived from monocytes that infiltrated the inflamed CNS and didn’t traffic to draining lymph nodes. Interestingly, during the course of their investigation, the authors also detected MBP– MHC complexes on oligodendrocytes (but not astrocytes or endothelial cells) of mice with EAE, and these cells triggered exvivo the production of IFN-c by T cells. Thus, under inflammatory conditions oligodendrocytes could be direct lytic targets of MBP-specific CD81 T cells and become a source of myelin debris or exosomes that will propagate the inflammatory response, including determinant spreading (Nat Immuno 2013; doi:10.1038/ni.2513).